Bronchus-Associated Lymphoid Tissue (BALT)

Randall, Troy D.

doi:10.1016/b978-0-12-381300-8.00007-1

Cited by 215 publications

(213 citation statements)

References 201 publications

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“…Differences between mouse and rat towards LPS treatment may be likely related to differences in their mucosal immune systems, such as the presence of BALT, and subsequently FAE in rats, but not in normal mouse. 43 In fact, TLR-4 and MHC Class II detected in bronchiolar FAE from control rats suggests that LPS uptake may occur in this compartment during the onset of lung inflammation. In parallel, we showed a predominant CD68 macrophage infiltrate in bronchioles, similar to another study, 44 but no lymphocytic or polymorphonuclear (neutrophilic) response was observed.…”

Section: Discussionmentioning

confidence: 99%

“…38 However, the close vicinity detected in our LPS model between bronchiole goblet cells and interstitial macrophages allow us to hypothesize that-beside any direct cell-cell interaction-soluble factors released by those macrophages may contribute also to modulate via a basolateral pathway the phenotype of bronchiolar goblet cells. Because of structural differences between the rat and human airway mucosal immune systems represented by the absence of BALT in healthy humans, 43 we decided to further validate our hypothesis in a human-based model rather than in rats stimulating in-vitro primary culture of HBEC with supernatants from human MDM challenged with or without LPS.…”

Section: Discussionmentioning

confidence: 99%

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Macrophages are related to goblet cell hyperplasia and induce MUC5B but not MUC5AC in human bronchus epithelial cells

Silva

Berčík

2012

Laboratory Investigation

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Airway goblet cell hyperplasia (GCH)-detectable by mucin staining-and abnormal macrophage infiltrate are pathological features present in many chronic respiratory disorders. However, it is unknown if both factors are associated. Using in-vivo and in-vitro models, we investigated whether macrophages are related with GCH and changes in mucin immunophenotypes. Lung sections from Sprague-Dawley rats treated for 48 h with one intra-tracheal dose of PBS or LPS (n ¼ 4-6 per group) were immunophenotyped for rat-goblet cells, immune, and proliferation markers. Human monocytederived macrophages (MDM) were pre-treated with or without LPS, immunophenotyped, and their supernatant, as well as cytokines at levels equivalent to supernatant were used to challenge primary culture of normal human bronchus epithelial cells (HBEC) in air-liquid interface, followed by MUC5B and MUC5AC mucin immunostaining. An association between increased bronchiolar goblet cells and terminal-bronchiolar proliferative epithelial cells confirmed the presence of GCH in our LPS rat model, which was related with augmented bronchiolar CD68 macrophage infiltration. The in-vitro experiments have shown that MUC5AC phenotype was inhibited when HBEC were challenged with supernatant from MDM pre-treated with or without LPS. In contrast, TNF-a and interleukin-1b at levels equivalent to supernatant from LPS-treated MDM increased MUC5AC. MUC5B was induced by LPS, supernatant from LPS-treated MDM, a mix of cytokines including TNF-a and TNF-a alone at levels present in supernatant from LPS-treated MDM. We demonstrated that macrophages are related with bronchiolar GCH, and that they induced MUC5B and inhibited MUC5AC in HBEC, suggesting a role for them in the pathogenesis of airway MUC5B-related GCH. KEYWORDS: airways; cytokines; LPS; lung inflammation; TNF-alphaMucus is a gel that covers the airway epithelium and is constituted by different glycoproteins called mucins, which are secreted by goblet cells from submucosal glands and the airway epithelium. 1 Mucus dissolves noxious gases and entraps foreign particles and pathogens, facilitating their clearance by mucociliary transport as a mechanism of innate defense. 2 However, in chronic inflammatory respiratory diseases, such as asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF), there is a pathological goblet cell hyperplasia (GCH) and mucus hypersecretion that can generate airway occlusion, associated with morbidity and death. 1 The main gel-forming mucins found in human airways are MUC5B and MUC5AC. 1 In healthy individuals, low levels of MUC5B and MUC5AC can be detected in mucus; although MUC5B is mainly present in the submucosal glands and MUC5AC is predominantly distributed in the airway epithelium. 3 In baseline conditions of chronic inflammatory respiratory disorders, MUC5B and/or MUC5AC are increased in different compartments of the respiratory tract. [3][4][5][6] For example, MUC5B and MUC5AC are augmented in small airway lumen and epithelium from patients with advanced CF; 4 GC...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Macrophages are related to goblet cell hyperplasia and induce MUC5B but not MUC5AC in human bronchus epithelial cells

Silva

Berčík

2012

Laboratory Investigation

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“…14,37 These lymphoid aggregates develop in response to chronic immune stimulation, which, in this case, may have been a Figures 13-14. Lymphoplasmacytic cuffs, lung, Norway rats.…”

Section: Discussionmentioning

confidence: 99%

Respiratory Pathology and Pathogens in Wild Urban Rats (Rattus norvegicus and Rattus rattus)

Rothenburger

Himsworth

Clifford³

et al. 2015

Vet Pathol

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Norway (Rattus norvegicus) and black rats (Rattus rattus) are common peridomestic species, yet little is known about wild rat ecology, including their natural diseases. We describe gross and histological lesions in the respiratory tract of a sample of 711 wild urban rats. A subset was examined for 19 distinct categories of histological lesions in the respiratory tract. Testing for known respiratory pathogens included serology and polymerase chain reaction (PCR) of lung samples. Grossly evident lesions were rare (8/711; 1%). Upper respiratory tract inflammation was present in 93 of 107 (87%) rats and included rhinitis, submucosal and periglandular lymphoplasmacytic tracheitis, and/or tracheal intraluminal necrotic debris and was significantly associated (P < .05) with the presence of cilia-associated respiratory bacillus (CARB), Mycoplasma pulmonis, and increased body mass (odds ratio [OR] ¼ 1.09; 95% confidence interval [CI] ¼ 1.05-1.14 per 10 g). Within the lungs, peribronchiolar and/or perivascular lymphoplasmacytic cuffs were present in 152 of 199 rats (76%) and were also significantly associated (P .02) with CARB, M. pulmonis, and increased body mass (OR ¼ 1.20; 95% CI ¼ 1.14-1.27 per 10 g). Rats were frequently coinfected with M. pulmonis and CARB, and lesions associated with these pathogens were histologically indistinguishable. Pneumocystis sp was detected in 48 of 102 (47%) rats using PCR but was not significantly associated with lesions. This description of pathology in the respiratory system of wild rats demonstrates that respiratory disease is common. Although the impact of these lesions on individual and population health remains to be investigated, respiratory disease may be an important contributor to wild rat morbidity and mortality.Keywords cilia-associated respiratory bacillus; lung; Mycoplasma pulmonis, pathology; Pneumocystis; rats; Rattus norvegicus; Rattus rattus; respiratory diseases; wild Norway and black rats (Rattus norvegicus and Rattus rattus) are cosmopolitan peridomestic species that are well adapted to living in urban habitats.12 Negative impacts of rats on human society range from economic losses through agricultural crop destruction to zoonotic diseases. 12,13,22 Even though rats have lived in cities with people for centuries, many details of urban rat ecology remain unexplored. Specifically, little is known about the causes of natural morbidity and mortality in rats.The life span of wild urban rats is considerably shorter than that of laboratory rats, with few individuals living beyond 1 year of age.12 Conversely, laboratory rats live up to 3 years. 43Factors contributing to the rapid population turnover among wild rats are unclear. Due to the high fecundity of rats, predation and human rat control activities, including trapping and poisoning, have limited effects on population size. 12 Mortality associated with resource competition does not explain why mature rats die, since they would be expected to outcompete juvenile rats.12 Natural disease may be a key component to

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“…Pulmonary infection in mice with pathogens such as influenza virus (9), murine herpesvirus 68 (12), Mycobacterium tuberculosis (31), modified vaccinia virus Ankara (32), or repetitive inhalations of heat-killed Pseudomonas aeruginosa (33) induced iBALT. These iBALTs contain myeloid DCs, a network of stromal cells, and FDCs within the B-cell follicles (12,32,34). The formation of HEVs and lymphatic vessels facilitates the recirculation of lymphocytes (35).…”

Section: Discussionmentioning

confidence: 99%

Thy1⁺IL-7⁺lymphatic endothelial cells in iBALT provide a survival niche for memory T-helper cells in allergic airway inflammation

Shinoda

Hirahara

Iinuma

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

103

100

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Memory CD4 + T helper (Th) cells are central to long-term protection against pathogens, but they can also be pathogenic and drive chronic inflammatory disorders. How these pathogenic memory Th cells are maintained, particularly at sites of local inflammation, remains unclear. We found that ectopic lymphoid-like structures called inducible bronchus-associated lymphoid tissue (iBALT) are formed during chronic allergic inflammation in the lung, and that memory-type pathogenic Th2 (Tpath2) cells capable of driving allergic inflammation are maintained within the iBALT structures. The maintenance of memory Th2 cells within iBALT is supported by Thy1 + IL-7-producing lymphatic endothelial cells (LECs). The Thy1 + IL-7-producing LECs express IL-33 and T-cell-attracting chemokines CCL21 and CCL19. Moreover, ectopic lymphoid structures consisting of memory CD4 + T cells and IL-7 + IL-33 + LECs were found in nasal polyps of patients with eosinophilic chronic rhinosinusitis. Thus, Thy1 + IL-7-producing LECs control chronic allergic airway inflammation by providing a survival niche for memory-type Tpath2 cells.

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Bronchus-Associated Lymphoid Tissue (BALT)

Cited by 215 publications

References 201 publications

Macrophages are related to goblet cell hyperplasia and induce MUC5B but not MUC5AC in human bronchus epithelial cells

Macrophages are related to goblet cell hyperplasia and induce MUC5B but not MUC5AC in human bronchus epithelial cells

Respiratory Pathology and Pathogens in Wild Urban Rats (Rattus norvegicus and Rattus rattus)

Thy1⁺IL-7⁺lymphatic endothelial cells in iBALT provide a survival niche for memory T-helper cells in allergic airway inflammation

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Bronchus-Associated Lymphoid Tissue (BALT)

Cited by 215 publications

References 201 publications

Macrophages are related to goblet cell hyperplasia and induce MUC5B but not MUC5AC in human bronchus epithelial cells

Macrophages are related to goblet cell hyperplasia and induce MUC5B but not MUC5AC in human bronchus epithelial cells

Respiratory Pathology and Pathogens in Wild Urban Rats (Rattus norvegicus and Rattus rattus)

Thy1+IL-7+lymphatic endothelial cells in iBALT provide a survival niche for memory T-helper cells in allergic airway inflammation

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Product

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Thy1⁺IL-7⁺lymphatic endothelial cells in iBALT provide a survival niche for memory T-helper cells in allergic airway inflammation